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PubMed2000

Pediatric obstructive sleep apnea syndrome.

Pediatric obstructive sleep apnea occurs in about 2% of children, and manifests as snoring, difficulty breathing, and witnessed apneic spells. Daytime symptoms include excessive sleepiness with poor performance and behavior problems. Severe forms may be associated with failure-to-thrive or death. The gold standard diagnostic procedure is overnight polysomnography and is indicated in high-risk patients. While most pediatric patients with obstructive sleep apnea can be treated with tonsillectomy and adenoidectomy; uvulopalatopharyngoplasty, tracheotomy, or other procedures are sometimes indicated. Nonsurgical treatment with continuous positive airway pressure is used in some children. Postoperative management in high-risk children includes careful perioperative monitoring and postoperative polysomnography.

Child↗

PubMed2006

Practice parameters for the medical therapy of obstructive sleep apnea.

Therapies for obstructive sleep apnea other than positive airway pressure, oral appliances, and surgical modifications of the upper airway are reviewed in this practice parameter. Several of these therapies such as weight loss and positional therapy hold some promise. Others, such as serotonergic agents, may gain credibility in the future but lack well-designed clinical trials. No practice parameters could be developed for a number of possible therapeutic modalities that had little or no evidence-based data on which to form a conclusion. The role of an organized, targeted weight-loss program either as a single therapy or as a supplement to PAP needs to be clarified. Although bariatric surgery is increasingly performed for refractory medically complicated obesity, its long-term effectiveness in treatment of obstructive sleep apnea in morbidly obese patients is not yet demonstrated. Positional therapy, or methods for preventing sleep in the supine position, has probably been underutilized due to lack of easily measured predictive factors and randomized controlled trials.

Combined Modality Therapy↗

PubMed2000

Sleep architectures of obstructive sleep apnea syndrome in the young child.

The sleep architectures of obstructive sleep apnea syndrome (OSAS) in the young child (child-OSAS, n = 17; mean age: 5.9+/-2.7 years; male:female 14:3) were compared with that of OSAS in the adult (n = 19; mean age: 44.7+/-10.7 years; male:female 18:1) and that of primary snoring in the child (n = 5; mean age: 7.0+/-2.4 years; male:female 5:0). Child-OSAS and OSAS in the adult had the same severity in oxygen desaturation. Child-OSAS showed lower Apnea-Hypopnea Index compared with OSAS in the adult. Sleep continuity in child-OSAS was not impaired compared with OSAS in the adult. Sleep fragmentation in child-OSAS was not so remarkable. The quantity of slow wave sleep in child-OSAS was similar to that of primary snoring in the child. Both profiles of sleep architectures showed nearly the same pattern.

Cerebral Cortex↗

PubMed2002

[Obstructive sleep apnea syndrome].

The obstructive sleep apnea syndrome (OSAS) is caused by an intermittent and repetitive obstruction of the upper respiratory tract during sleep, which leads to a complete (apnea) or partial (hypopnea) block of air flow. It is quite prevalent, being seen in 4-6% of males and 2% of females. Structural abnormalities present in the upper respiratory tract and obesity are the fundamental etiological factors. Clinical manifestations are due to sleep fragmentation and oxygen desaturation which cause the apnea. Day hypersomnia, snoring and episodes of apnea described by the spouse are the three basic symptoms. The diagnosis is based on polysomnography, which can be substituted for a night cardiorespiratory polygraphy. It has an important morbimortality rate, mainly due to traffic and labor accidents, ischemic heart disease and chronic respiratory failure. The treatment is multifactorial. First, eliminating alcohol and hypnotic drugs. Obesity, which is almost always present, must also be corrected. Structural abnormalities of the upper respiratory tract may require a surgical solution. The treatment preferred nowadays is the application of a nasal continuous positive airway pressure (CPAP) while the patient is asleep. It should be considered for those symptomatic patients with an apnea-hypopnea index over 30, or if the index is below 30, than when a respiratory insufficiency or cardiovascular risk factors are present. In some cases surgical procedures may be considered, such as uvulopalatopharyngoplasty.

Female↗

PubMed1999

Snoring and obstructive sleep apnea.

The most common form of sleep apnea is obstructive sleep apnea (OSA). It is characterized by the cessation of nasal airflow with persistence of ventilatory effort, as shown by paradoxical chest and abdominal movement, and varying degrees of oxygen desaturation. This article describes current methods of diagnosing OSA and available treatment for OSA and snoring.

Humans↗

PubMed1988

Mortality and apnea index in obstructive sleep apnea. Experience in 385 male patients.

Although obstructive sleep apnea (OSA) has been studied in detail for over a decade, the mortality of this disorder is unclear. We calculated cumulative survival in 385 male OSA patients. We found that those with an apnea index (AI) greater than 20 had a much greater mortality than those with AI = less than 20. The probability of cumulative eight-year survival was .96 +/- 0.02 (SE) for AI = less than 20 vs. 63 +/- 0.17 for AI greater than 20 (p less than .05). This difference in mortality related to AI was particularly true in the patients less than 50 years of age in whom mortality from other causes is not common. None of the patients treated with tracheostomy or nasal CPAP died. Eight of the patients treated with uvulopalatopharyngoplasty (UPPP) died and the cumulative survival of the UPPP-alone treated group was not different from the survival curve of untreated OSA patients with an apnea index of greater than 20. We conclude that OSA patients with an apnea index of greater than 20 have a greater mortality than those below 20 and that UPPP patients be restudied after therapy. If the latter patients are found not to have marked amelioration of their AI, then they should be treated by nasal CPAP or tracheostomy.

Actuarial Analysis↗

PubMed1995

Energy expenditure in obstructive sleep apnea.

Patients with obstructive sleep apnea (OSA) are often obese and, in common with obese patients generally, find it difficult to lose weight. Obstructive sleep apnea may be associated with changes in total daily energy expenditure that could contribute to obesity and complicate its management. To determine whether resting metabolic rate and the thermogenic effect of food are reduced in OSA, we have compared postabsorptive resting energy expenditure (REE) and dietary thermogenesis (DT) in 14 patients with moderate to severe symptomatic OSA and 14 control subjects matched for obesity. Anthropometrics, body composition analysis using bioelectrical impedance and indirect calorimetry using a metabolic cart and canopy system were performed in all subjects. Dietary thermogenesis after a liquid meal equivalent to 35% of REE was measured in 13 patients and 8 control subjects. Measurements were repeated after chronic (mean +/- SD 12 +/- 5 weeks) nasal continuous positive airway pressure (CPAP) therapy in 10 patients with OSA. Energy expenditure was expressed in terms of metabolic body size. The patients with OSA were heavier and had larger necks and a larger lean body mass (LBM) than controls, but the two groups were well matched for body mass index (BMI) and percent body fat. REE was greater in OSA patients than controls, but when corrected for LBM there was no difference between the two groups (27 +/- 3 vs. 28 +/- 4 kcal/kg). DT was similar in patients and controls (17 +/- 6 vs. 15 +/- 10%). REE/LBM was quite consistent among patients with OSA, regardless of body weight. REE and DT did not change following chronic nasal CPAP therapy. (ABSTRACT TRUNCATED AT 250 WORDS)

Anthropometry↗

PubMed2005

Chronic liver injury during obstructive sleep apnea.

Patients with obstructive sleep apnea (OSA) are at risk for the development of fatty liver as a result of being overweight. Several data suggest that OSA per se could be a risk factor of liver injury; ischemic hepatitis during OSA has been reported, and OSA is an independent risk factor for insulin resistance. Therefore, we investigated liver damage and potential mechanisms in 163 consecutive nondrinking patients with nocturnal polysomnographic recording for clinical suspicion of OSA. Serum levels of liver enzymes were measured in all patients. Liver biopsy was offered to patients with elevated liver enzymes. Intrahepatic hypoxia was assessed by the expression of vascular endothelial growth factor (VEGF) on liver biopsy specimens. Severe OSA (apnea-hypopnea index [AHI] > 50/hr) was seen in 27% of patients; 52% had moderate OSA (AHI 10-50/hr), and 21% had no OSA. Overall, 20% had elevated liver enzymes. Independent parameters associated with elevated liver enzymes were body mass index (BMI) (OR: 1.13; CI: 1.03-1.2) and severe OSA (OR: 5.9; CI: 1.2-29). Liver biopsy was performed in 18 of 32 patients with elevated liver enzymes and showed steatohepatitis in 12 cases, associated with fibrosis in 7 cases. Patients with severe OSA were more insulin-resistant according to homeostasis model assessment, had higher percentage of steatosis as well as scores of necrosis and fibrosis, despite similar BMI. Hepatic immunostaining used as an indirect marker of hypoxia was not different between patients with or without severe OSA. In conclusion, severe OSA is a risk factor for elevated liver enzymes and steatohepatitis independent of body weight. Promotion of insulin resistance is probably involved. Further studies are needed to determine whether hypoxia contributes directly to liver injury.

Adult↗

PubMed2005

Preoperative evaluation of patients with obesity and obstructive sleep apnea.

Obesity and obstructive sleep apnea are conditions frequently encountered by the anesthesiologist and may have a significant impact on perioperative outcomes. This article discusses the preoperative evaluation of patients with one or both of these conditions. The goals of the preoperative assessment are to identify issues that can adversely affect the patient. This information is critical to forming an effective plan for the perioperative care of the patient.

Humans↗

PubMed2005

Serum homocysteine levels and cardiovascular morbidity in obstructive sleep apnea syndrome.

BACKGROUND: Obstructive sleep apnea syndrome (OSAS) is associated with cardiovascular morbidity and mortality. Elevated levels of serum homocysteine are also associated with cardiovascular morbidity and mortality. We aimed to investigate serum homocysteine levels and conventional cardiovascular risk factors (cholesterol, low-density lipoprotein (LDL), high-density lipoprotein (HDL), triglycerides) in OSAS patients with and without cardiovascular diseases (CVD). METHODS AND RESULTS: Levels of homocysteine, cholesterol, LDL, HDL and triglycerides were measured in 114 obese, male participants after overnight fasting. The presence of OSAS was determined by standard overnight polysomnography. The cases included OSAS patients (apnea-hypopnea index: AHI5) with CVD (OSAS+CVD group) (n:25) and without CVD (OSAS-CVD group) (n:47). Control group was patients without OSAS (AHI<5) with CVD (CVD group) (n:42). The serum homocysteine levels were significant.

Adult↗

PubMed2000

Neural and humoral mechanisms mediating cardiovascular responses to obstructive sleep apnea.

Patients with obstructive sleep apnea are at increased risk for hypertension. The mechanisms underlying this increased risk are not known. During sleep, repetitive apneic episodes result in hypoxemia and carbon dioxide retention, which cause increases in sympathetic nerve activity and elicit humoral vasoconstrictor responses. While these mechanisms explain nocturnal elevations in blood pressure, it is unclear why hypertension and elevated sympathetic nerve activity prevail even during the daytime. This review will examine briefly some of the neural and humoral mechanisms that are activated by nocturnal apneas and which may contribute to persistent increases in blood pressure even during daytime normoxia. Disruption of the autonomic and hemodynamic profile of normal sleep by apneic events manifests as raised blood pressure and heightened sympathetic nerve traffic during sleep. During awake daytime normoxia, baroreflex and chemoreflex dysfunction may contribute to maintenance of higher blood pressure and sympathetic activity. Sustained vasoconstrictor effects of nocturnal endothelin release may also be implicated in the elevated daytime blood pressures.

Animals↗

PubMed2003

Obstructive sleep apnea in epilepsy.

Obstructive sleep apnea can affect an individual with epilepsy profoundly. These relatively common disorders can coexist and potentially exacerbate each other. The identification and appropriate treatment of OSA may have far-reaching consequences in improving a patient's quality of life and recurrence of seizures. Clinicians must be aware of the relationship of these disorders and keenly question epilepsy patients, regardless of their body habitus, regarding potential symptoms of sleep apnea. Although the underlying pathogenic mechanisms are unclear, we can model the information gained from the observations to further the understanding of the relationship between sleep and epilepsy.

Clinical Trials as Topic↗

PubMed2003

Indications for treatment of obstructive sleep apnea in adults.

Obstructive sleep apnea is associated with significant daytime sleepiness, reduced quality of life, insulin resistance, motor vehicle crashes, vascular morbidity and mortality. Current evidence supports the belief that all these parameters can be impacted favorably by treatment. Medical therapy with positive pressure eliminates snoring and favorably affects daytime sleepiness, driving risk, vascular function, vascular risk, and quality of life. Treatment may be difficult to accept or adhere to, and some treatment options are not uniformly effective. The long-term impact of treatment is uncertain.

Adult↗

PubMed2003

Antioxidant capacity in obstructive sleep apnea patients.

OBJECTIVES: Obstructive sleep apnea syndrome (OSA) results in oxygen desaturation and arousal from sleep. Free oxygen radicals are highly reactive molecules, which can be produced by the OSA phenomenon known as hypoxia/reoxygenation. Hypoxic conditions, such as OSA, may also result in transient depletion of cellular reductants, which constitute a main line of antioxidant defense. Both apneas and hypopneas usually end in arousal, where reoxygenation causes the production of reactive oxygen species (free radicals). Living organisms have developed complex antioxidant systems to counteract reactive oxygen species and to reduce their damage. We evaluated the antioxidant capacity in serum from OSA patients and healthy people in order to confirm the hypothesis that there is a relationship between oxidative stress and OSA. MATERIALS AND METHODS: A physician interviewed 25 participants, determining age, smoking habits and symptoms such as excessive daytime sleepiness and snoring. Physical examination and polysomnography were performed during patients' hospitalization. Antioxidant capacity was measured in blood samples by Trolox Equivalent Antioxidant Capacity assay. RESULTS: Seventeen out of 25 subjects had an apnea/hypopnea index (AHI) greater than 10 (OSA group). The measurement of antioxidant capacity did not differ between the OSA patients and our healthy sample (of 25 subjects, seven with an AHI less than 10). Furthermore, patients with severe OSA (AHI >20, N=14) had linearly negative correlation between antioxidant capacity in their blood samples and AHI (R=-0.551, P=0.041). CONCLUSIONS: Reduced antioxidant capacity in serum is an index of excessive oxidative stress. Patients with severe OSA have reduced values of antioxidant capacity.

Adult↗

PubMed2002

A whole-genome scan for obstructive sleep apnea and obesity.

Obstructive sleep apnea (OSA) is a common, chronic, complex disease associated with serious cardiovascular and neuropsychological sequelae and with substantial social and economic costs. Along with male gender, obesity is the most characteristic feature of OSA in adults. To identify susceptibility loci for OSA, we undertook a 9-cM genome scan in 66 white pedigrees (n=349 subjects) ascertained on the basis of either an affected individual with laboratory-confirmed OSA or a proband who was a neighborhood control individual. Multipoint variance-component linkage analysis was performed for the OSA-associated quantitative phenotypes apnea-hypopnea index (AHI) and body mass index (BMI). Candidate regions on chromosomes 1p (LOD score 1.39), 2p (LOD score 1.64), 12p (LOD score 1.43), and 19p (LOD score 1.40) gave the most evidence for linkage to AHI. BMI was also linked to multiple regions, most significantly to markers on chromosomes 2p (LOD score 3.08), 7p (LOD score 2.53), and 12p (LOD score 3.41). Extended modeling indicated that the evidence for linkage to AHI was effectively removed after adjustment for BMI, with the exception of the candidate regions on chromosomes 2p (adjusted LOD score 1.33) and 19p (adjusted LOD score 1.45). After adjustment for AHI, the primary linkages to BMI remained suggestive but were roughly halved. Our results suggest that there are both shared and unshared genetic factors underlying susceptibility to OSA and obesity and that the interrelationship of OSA and obesity in white individuals may be partially explained by a common causal pathway involving one or more genes regulating both AHI and BMI levels.

Adult↗

PubMed2006

Obesity-related cardiovascular disease: implications of obstructive sleep apnea.

Obesity and obstructive sleep apnea (OSA) often coexist. OSA has been linked to cardiovascular disease. Thus, OSA may contribute to the cardiovascular consequences of obesity. In this review, we explore clinical and pathophysiological interactions between obesity, cardiovascular disease and OSA. We discuss the mechanisms whereby OSA may contribute to hypertension, atherosclerosis, insulin resistance and atrial fibrillation associated with obesity, and emphasize the potential implications for understanding why only a subgroup of obese patients develop cardiovascular disease. Identification of the OSA-dependent and OSA-independent pathways in the cardiovascular pathophysiology of obesity may hold clinical and therapeutic promise.

Atherosclerosis↗

PubMed2000

Increases in leptin levels, sympathetic drive, and weight gain in obstructive sleep apnea.

Patients with obstructive sleep apnea (OSA) are frequently obese and are predisposed to weight gain. They also have heightened sympathetic drive. We reasoned that noradrenergic activation of beta(3)-receptors on adipocytes would inhibit leptin production, predisposing to obesity in sleep apnea. We therefore tested the hypothesis that obesity and predisposition to weight gain in OSA are associated with low levels of plasma leptin. We prospectively studied 32 male patients (43 +/- 2 yr) with OSA who were newly diagnosed and never treated and who were free of any other diseases. Control measurements were obtained from 32 similarly obese closely matched male subjects (38 +/- 2 yr). Leptin levels were 13.7 +/- 1.3 and 9.2 +/- 1.2 ng/ml in patients with OSA and controls, respectively (P = 0.02). Weight gain over the year before diagnosis was 5.2 +/- 1.7 and 0.5 +/- 0.9 kg in sleep apnea patients and similarly obese control subjects, respectively (P = 0.04). Muscle sympathetic activity was 46 +/- 4 and 30 +/- 4 bursts/min in patients with OSA (n = 16) and control subjects (n = 18), respectively (P = 0.01). Plasma leptin levels are elevated in newly diagnosed otherwise healthy patients with untreated sleep apnea beyond the levels seen in similarly obese control subjects without sleep apnea. Higher leptin levels in OSA, independent of body fat content, suggest that OSA is associated with resistance to the weight-reducing effects of leptin.

Adult↗

PubMed2006

Circulating ICAM-1 and VCAM-1 levels in patients with obstructive sleep apnea syndrome.

BACKGROUND: Obstructive sleep apnea syndrome (OSAS)-induced hypoxic stress modulates circulating inflammatory mediators causing accelerated atherogenesis. OBJECTIVES: We hypothesized that OSAS-induced hypoxia might result in cardiovascular disease due to increased expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) on the endothelial surface. METHODS: Thirty-nine subjects with moderate-to-severe OSAS and 34 non-apneic controls matched for age, gender, body mass index (BMI), smoking history, and cardiovascular disease were included in this prospective study. Overnight polysomnography was performed. Circulating ICAM-1 and VCAM-1 levels in the serum were measured by enzyme-linked immunosorbent assay. RESULTS: Circulating levels of both ICAM-1 (480.1 +/- 216.7 vs. 303.4 +/- 98.6 ng/ml, p < 0.0001) and VCAM-1 (1,156.6 +/- 79.8 vs. 878.8 +/- 71.1 ng/ml, p = 0.002) were significantly increased in the OSAS group compared to the control group. For an ICAM-1 cutoff level of 375 ng/ml, predictive sensitivity and specificity for OSAS were 69.2% (95% confidence interval, CI: 52.4-83.0%) and 82.4% (95% CI: 65.5-93.2%), respectively. For a VCAM-1 cutoff level of 859 ng/ml, predictive sensitivity and specificity for OSAS were 74.4% (95% CI: 57.9-86.9%) and 64.7% (95% CI: 46.5-80.2%), respectively. There was a significant positive correlation between circulating levels of ICAM-1 and ln of AHI (r = 0.276, p = 0.018). Multiple logistic regression analyses showed that OSAS was associated with high ICAM-1 and high VCAM-1 levels independent of age, gender, BMI, smoking status and cardiovascular disease. CONCLUSION: We conclude that OSAS can independently increase circulating levels of adhesion molecules

Adult↗